NGF-induced remodeling of mature uninjured axon collaterals

Accumulation of nerve growth factor (NGF) within the rat hippocampus following septal denervation is thought to contribute to sympathetic axon ingrowth. However, intraventricular NGF infusion, which results in elevated hippocampal NGF, fails to elicit such sprouting, although it increases innervation of the extracerebral vasculature. To determine whether or not NGF would stimulate sympathohippocampal sprouting, we infused NGF after sprouting was initiated. Surprisingly, NGF reduced the amount of hippocampal sprouting and, when infused at the time of lesion, delayed its onset while, at the same time, stimulating perivascular sprouting. Since NGF did not prevent ingrowth into the hippocampus from transplanted sympathetic ganglia, the reduction in sympathetic hippocampal fibers from intact ganglia appears to result from the proliferation of vascular fibers. Thus, changes in trophic support (NGF levels) appear to be sufficient to produce remodeling of mature, uninjured sympathetic arbors. Such trophomorphism may underlie collateral elimination during normal development and injury-induced neuronal rearrangements.